Effects of anesthesia on the canine carotid chemoreceptor reflex

We studied the effects of α-chloralose (100 mg/kg, iv), Na pentobarbital (25 mg/kg, iv) and halothane (1 vol% and 2 vol%) on the response to carotid chemoreceptor stimulation (CCRS) in eight chronically instrumented dogs. CCRS was accomplished by means of intracarotid injections of nicotine while ventilation was held constant in the unanesthetized state and following administration of one of three different anesthetics. In the conscious state, CCRS elicited intense bradycardia and peripheral vasoconstriction as reflected by a 173 ± 14% increase in initial cardiac cycle length and a 216 ± 22% increase in mean iliac vascular resistance. Each anesthetic, studied on separate days, attenuated these responses to CCRS strikingly (P < 0.01). For instance, after α-chloralose, CCRS increased iliac resistance by only 55 ± 14% and cardiac cycle length by only 27 ± 13%. After Na pentobarbital, CCRS increased iliac resistance by 12 ± 4% and cardiac cycle length by 8 ± 5%. After inhalation of halothane (1 vol%), CCRS increased iliac resistance by 28 ± 7/% and cardiac cycle length by 11 ± 5%, whereas halothane (2 vol%) abolished these responses to CCRS. Thus, general anesthesia interferes severely with carotid chemoreceptor control of the circulation. Whereas halothane and Na pentobarbital altered responses to CCRS the most, we found that even α-chloralose, which has been thought to maintain or augment reflex responses, was able to depress the response to CCRS strikingly.